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Abstract
The pathogenesis of NO 2 ‐induced respiratory disease and the effect of NO 2 on respiratory clearance of s1Cr 2 O i were studied. Young adult female mice were exposed to a 51Cr 2 O 3 aerosol, followed by a daily exposure to either 30 ppm NO 2 for 2 wk or 60 ppm NO 2 for 2 wk or a single exposure to 170 ppm NO 2 . Exposure to 30 ppm NO 2 had a minimal histopathologic effect on respiratory tract tissue. Exposure to 60 ppm NO 2 produced marked histopathologic effects, which were subsequently resolved. Exposure to 170 ppm NO 2 produced permanent histopathologic lesions.
In mice exposed to concentrations of NO 2 that produced minimal histopathologic effects, respiratory clearance of 51 Cr 2 O 3 was similar to that in unexposed mice. When mice were exposed to concentrations of NO 2 that produced permanent tissue damage, prolonged impairment of respiratory clearance of 51 Cr 2 O 3 was observed, despite resolution of edema produced by inhalation of NO 2 . At concentrations of NO 2 that produced marked edema and histopathologic effects that were resolved despite repeated N0 2 exposure, there was an initial marked impairment of respiratory clearance, then an accelerated rate of clearance, and finally a clearance rate similar to that of unexposed mice. The time during which accelerated clearance occurred was well correlated with the time at which the histopathologic lesion was observed to regress.